Prostaglandins & other lipid mediators最新文献

{"title":"Effects of statin use on blood pressure and other hypertension-related outcome indicators in hypertensive patients: A systematic review and meta-analysis","authors":"Zhaohan Chu ,&nbsp;Wei Yue ,&nbsp;Qingqing Mu ,&nbsp;Dong Xu ,&nbsp;Zexu Chang ,&nbsp;Mengke Liang ,&nbsp;Yixiao Geng ,&nbsp;Ping Ding","doi":"10.1016/j.prostaglandins.2025.106991","DOIUrl":"10.1016/j.prostaglandins.2025.106991","url":null,"abstract":"<div><h3>Aims</h3><div>This meta-analysis delved into the impact of statin therapy, both as a monotherapy and in conjunction with antihypertensive medications, on blood pressure levels and outcomes pertinent to hypertension.</div></div><div><h3>Methods</h3><div>We searched the PubMed, EMBASE, and Cochrane databases for studies published before October 1 2023. Studies designed as cohort studies or randomized controlled trials and investigating the effects of single use of statin or its combined use with other antihypertensive therapy were included. Authors extracted the data independently and differences were decided through discussion. Random-effects model was used to evaluate the merged outcomes. Due to the high heterogeneity of the HDL-C group, we performed subgroup analysis according to the type of statin. To assess the robustness and potential publication bias of our findings, we utilized sensitivity analysis, Egger’s test, and funnel plots.</div></div><div><h3>Results</h3><div>23 trials were included in this meta-analysis. The primary outcomes revealed that administering statins did not significantly impact the systolic pressure (SBP) of hypertensive patients (MD, −1.77; 95 % CI, −4.82–1.27). —The promoted effect of statin treatment on diastolic pressure (DBP) in hypertensive patients was found (MD, −1.87; 95 % CI, −3.72 –-0.01). The secondary outcomes revealed that the use of statins resulted in a significant reduction in low-density lipoprotein (LDL-C), while significantly increasing high-density lipoprotein (HDL-C) in hypertensive patients.</div></div><div><h3>Conclusion</h3><div>Statin use did not modulate SBP and DBP of patients with hypertension, but SBP was decreased in the rosuvastatin or pravastatin subgroup, while DBP was decreased in the simvastatin or pravastatin subgroup. Statin treatment reduced LDL-C, increased HDL-C, and reduced the incidence of cardiovascular events and mortality compared to control groups.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106991"},"PeriodicalIF":2.5,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143773212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased plasma lipoxin A4, resolvin D1, protectin D1 are correlated with the complexity and prognosis of coronary heart disease: A retrospective cohort study","authors":"Yun-fei Wang ,&nbsp;Xue-tao Zhu ,&nbsp;Ze-ping Hu","doi":"10.1016/j.prostaglandins.2025.106990","DOIUrl":"10.1016/j.prostaglandins.2025.106990","url":null,"abstract":"<div><div>This study aimed to assess the predictive capacity of specialized pro-resolving mediators (SPMs) regarding the complexity and prognosis of coronary heart disease (CHD). Total of 602 CHD patients were included in this study and categorized into low-risk, medium-risk, and high-risk groups based on the Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery (SYNTAX) score. Follow-up was conducted for two years, during which patients were dichotomized into poor and good prognosis groups. Additionally, twenty healthy controls were incorporated. Plasma concentrations of lipoxin A4 (LXA4), resolvin D1 (RvD1), protectin D1 (PD1), C-reactive protein (CRP), interleukin-6 (IL-6), and IL-10 were quantified. Plasma LXA4, RvD1, PD1, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 exhibited a gradual decrease across control, low-risk, medium-risk, and high-risk groups and exhibited a negative correlation with the SYNTAX score. Spearman’s correlation analysis revealed negative correlations between plasma LXA4, RvD1, PD1, and both CRP and IL-6, and positive correlations with IL-10. Multiple linear regression models demonstrated negative associations between plasma LXA4, RvD1, PD1, and SYNTAX score. Moreover, both univariate and multivariate binary logistic regression analyses identified plasma LXA4, RvD1, and PD1 as protective factors against medium/high-risk SYNTAX score categorization. In the poor prognosis group, plasma PD1 was reduced at short-term follow-up, and the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were reduced at long-term follow-up. Plasma LXA4, RvD1, and PD1 demonstrated negative correlations with CHD complexity and potentially served as protective factors against CHD. Plasma PD1 provided predictive value for short-term prognosis, while the ratios LXA4/IL-6, RvD1/IL-6, PD1/IL-6 were indicative for long-term prognosis.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106990"},"PeriodicalIF":2.5,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E2F7 upregulates MCM4 and fatty acid metabolism to advance lung adenocarcinoma metastasis","authors":"WuAsen Tang ,&nbsp;Deming Zhang ,&nbsp;Di Liu,&nbsp;Zikang Liu,&nbsp;Kuang Xiao,&nbsp;Chenggang Lei,&nbsp;Yalun Yang,&nbsp;Qian Zhou,&nbsp;Xianghui Wang","doi":"10.1016/j.prostaglandins.2025.106988","DOIUrl":"10.1016/j.prostaglandins.2025.106988","url":null,"abstract":"<div><h3>Background</h3><div>MCM4, a key protein in MCM, is frequently overexpressed in cancers, but its specific role in lung adenocarcinoma (LUAD) metastasis is unclear.</div></div><div><h3>Methods</h3><div>Bioinformatics revealed the mRNA expression pattern of MCM4 in LUAD, which we confirmed in both normal lung epithelial and adenocarcinoma cell lines using qRT-PCR and western blot (WB). Cellular proliferation was gauged by cell counting kit-8 and colony formation assays, and the expression of epithelial-mesenchymal transition markers along with fatty acid synthase (FASN) was probed via WB. We employed Transwell to assess cellular migration and invasion, and utilized kits for quantifying intracellular triglycerides and phospholipids. Bioinformatics identified E2F7 as a potential transcriptional regulator of MCM4, prompting us to explore its relationship with MCM4, including predicted binding sites and E2F7 mRNA expression in LUAD. Chromatin immunoprecipitation and dual-luciferase reporter assays were conducted to validate the regulatory effects of E2F7 on MCM4.</div></div><div><h3>Results</h3><div>MCM4 was found to be overexpressed in LUAD, and its knockdown inhibited cancer cell proliferation, migration, invasion, and metastasis, along with decreased FASN expression and declined levels of triglycerides and phospholipids within cells. Mechanistically, E2F7 transcriptionally activated MCM4, regulating fatty acid metabolism and promoting LUAD progression and metastasis.</div></div><div><h3>Conclusion</h3><div>Our study elucidates the mechanism by which E2F7 transcriptionally controls MCM4 to activate fatty acid metabolism, fueling LUAD metastasis. These discoveries emphasize the pivotal function of lipid metabolism in LUAD development and suggests new therapeutic targets for LUAD treatment.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106988"},"PeriodicalIF":2.5,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of adipose TGF-β1 by probiotics alleviates metabolic disturbance in experimentally induced PCOS","authors":"Kehinde S. Olaniyi ,&nbsp;Doris O. Okara,&nbsp;Stephanie E. Areloegbe","doi":"10.1016/j.prostaglandins.2025.106989","DOIUrl":"10.1016/j.prostaglandins.2025.106989","url":null,"abstract":"<div><h3>Background</h3><div>Polycystic ovarian syndrome (PCOS) is critically characterized with metabolic and endocrine dysfunctions, precipitating metabolic syndrome and infertility in reproductive aged women. Adipose tissue dysfunction has been implicated in the pathogenesis of metabolic syndrome, including in PCOS individuals. Probiotics are healthy bacteria in the gut that regulate metabolic health. However, the impact of probiotics on adipose-driven metabolic syndrome has not been reported. The present study therefore hypothesized that probiotics would attenuates metabolic disturbance in experimental PCOS rat model, probably by suppression of TGF-β1.</div></div><div><h3>Materials and methods</h3><div>Eight-week-old female Wistar rats were randomly allotted into four groups (n = 5). Administration of letrozole (1 mg/kg <em>p.o</em>) for 21 days induced PCOS, thereafter the animals were treated with 3x10⁹ CFU (<em>p. o</em>) of probiotics for six weeks.</div></div><div><h3>Results</h3><div>Letrozole-induced PCOS rats were characterized with elevated circulating testosterone, and multiple ovarian cysts. In addition, rats with PCOS developed increased body weight, which was also accompanied with insulin resistance, hyperinsulinemia, and increased leptin, and decreased adiponectin and adipose TG, as well as elevated adipose lipase. Inflammatory markers (NF-kB, TNF-α) were elevated, while antioxidant defense (GSH) was depleted in PCOS animals. A significant increase in adipose TGF-β1, caspase-6 and HDAC2 levels was observed in PCOS rats when compared with the control. Immunohistochemical evaluation of adipose tissue also showed severe expression of NLRP3 in PCOS rats and these changes were accompanied by increased level of TGF-β1. However, treatment with probiotics reversed these aberrant systemic and adipose tissue changes in PCOS model.</div></div><div><h3>Conclusion</h3><div>The present results suggest the therapeutic benefit of probiotics against metabolic disturbance in PCOS model through suppression of TGF-β1-dependent pathway.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106989"},"PeriodicalIF":2.5,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143716315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ceramide and DNA damage in liver fibrosis: Exploring the implications of eicosapentaenoic acid encapsulation in cellulose nanocrystals","authors":"Jihan Hussein ,&nbsp;Mona A. El-Bana ,&nbsp;Rehab A. Mohamed ,&nbsp;Enayat Omara ,&nbsp;Dalia Medhat","doi":"10.1016/j.prostaglandins.2025.106985","DOIUrl":"10.1016/j.prostaglandins.2025.106985","url":null,"abstract":"<div><div>Ceramide plays a crucial role in promoting liver fibrosis by inducing apoptosis and inflammation in hepatocytes. Oxidative stress accelerates fibrosis by elevating levels of urinary 8-hydroxy-2′-deoxyguanosine (8-OHdG), an indicator for the damage of DNA. We aimed to evaluate the efficacy of eicosapentaenoic acid encapsulated in cellulose nanocrystals (EPA-CNC) in inhibiting ceramide accumulation and reducing urinary 8-OHdG levels, thus providing protective effects against the progression of liver fibrosis.</div><div>In this study, twenty-four adult male Wistar albino rats were allocated into a negative control group, a group with liver fibrosis induced by diethylnitrosamine (DEN), and a group with DEN-induced liver fibrosis treated simultaneously with EPA-CNC. Key parameters assessed included liver paraoxonase-1 (PON-1), plasma interleukin-6 (IL-6), plasma ceramide, liver hydroxyproline (Hyp) content, and urinary 8-OHdG.</div><div>DEN-induced liver fibrosis led to a significant increase in inflammatory markers, including ceramide, IL-6, and notably urinary 8-OHdG. This was accompanied by a decrease in PON-1 activity and increased collagen deposition in liver tissues (Hyp content). Histopathological analysis revealed a substantial loss of liver architecture, with inflammation and fibrosis surrounding necrotic areas.</div><div>In contrast, treatment with encapsulated EPA-CNC resulted in a significant decrease in plasma ceramide, IL-6, liver Hyp content, and urinary 8-OHdG levels, along with an improvement in liver PON-1 activity. Histopathological findings showed nearly normal liver architecture.</div><div>In conclusion, increased levels of ceramide and urinary 8-OHdG could serve as indicators of ongoing hepatocellular damage due to their positive correlations with fibrotic markers. Encapsulated EPA-CNC may offer a promising approach for halting oxidative stress and inflammation in liver fibrosis.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"178 ","pages":"Article 106985"},"PeriodicalIF":2.5,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Menaquinone-7 (MK-7) Supplementation on Anthropometric Measurements, Glycemic Indices, and Lipid Profiles: A Systematic Review and Meta-Analysis of Randomized Controlled Trials","authors":"Omid Nikpayam ,&nbsp;Ali Jafari ,&nbsp;Amirhossein Faghfouri ,&nbsp;Mohammadjavad Pasand ,&nbsp;Pardis Noura ,&nbsp;Marziyeh Najafi ,&nbsp;Golbon Sohrab","doi":"10.1016/j.prostaglandins.2025.106970","DOIUrl":"10.1016/j.prostaglandins.2025.106970","url":null,"abstract":"<div><h3>Background</h3><div>Menaquinone-7 (MK-7) is a type of vitamin K that has a longer half-life and stays in the body for a more extended period compared to other types of vitamin K. Recently, the effects of this vitamin on body weight, glycemic control, and lipid profiles have garnered much attention. <strong>Aim of the review:</strong> This systematic review and meta-analysis were performed to evaluate the effects of MK-7 on anthropometric measurements, glycemic indices, and lipid profiles.</div></div><div><h3>Methods</h3><div>A systematic search via appropriate keywords was conducted in electronic databases including PubMed, Scopus, Web of Science, and Google Scholar up to October 2023 to obtain relevant original articles. The quality of studies was evaluated using the Cochrane Collaboration tool. Six original articles met our criteria and were included in the analysis.</div></div><div><h3>Results</h3><div>Statistical analysis showed that MK-7 had a desirable effect on inulin (SMD= −0.56; 95 % CI: −0.77, −0.36; P = 0.000, I2 = 84 %, P = 0.000), HbA1c (SMD=-0.32; 95 % CI: −0.55, −0.09; P = 0.007, I2 = 86.8 %, P = 0.000), and homeostatic Model Assessment for Insulin Resistance (HOMA-IR) (SMD= −0.56; 95 % CI: −0.76, −0.35; P = 0.000, I2 = 84.3 %, P = 0.000). Additionally, subgroup analysis revealed negligible effects of MK-7 on total cholesterol (TC), insulin, HbA1c, and HOMA-IR in both genders of patients who received ≤ 90 mg MK-7 for less than 12 weeks. However, MK-7 didn’t have any meaningful effect on other factors.</div></div><div><h3>Conclusion</h3><div>Based on the findings of the present systematic review and meta-analysis, MK-7 may have beneficial effects on glycemic control and TC, although further highly qualified original research is needed for a consistent conclusion.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106970"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An editorial farewell","authors":"Michal Laniado Schwartzman","doi":"10.1016/j.prostaglandins.2025.106950","DOIUrl":"10.1016/j.prostaglandins.2025.106950","url":null,"abstract":"","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106950"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143010771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The interplay of LDLR, PCSK9, and lncRNA- LASER genes expression in coronary artery disease: Implications for therapeutic interventions","authors":"Tayebe Ghiasvand ,&nbsp;Jamshid Karimi ,&nbsp;Iraj Khodadadi ,&nbsp;Amirhossein Yazdi ,&nbsp;Salman Khazaei ,&nbsp;Zahra Abedi kichi ,&nbsp;Seyed Kianoosh Hosseini","doi":"10.1016/j.prostaglandins.2025.106969","DOIUrl":"10.1016/j.prostaglandins.2025.106969","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Coronary artery disease (CAD) is defined as stenosis of coronary arteries due to atherosclerosis. The etiology of atherosclerosis can be attributed to a disruption in lipid metabolism, specifically cholesterol and low-density lipoprotein cholesterol (LDL-C). PCSK9 is an enzyme that controls the metabolism of LDL-C by degrading the low-density lipoprotein receptor (LDLR), which in turn affects the metabolism of LDL-C. A newly discovered Long Non-coding RNA named <em>LASER</em>, which affects the homeostasis of cholesterol, has been identified through the evaluation of bioinformatics. The objective of this study was to assess the levels of gene expression related to cholesterol balance, specifically <em>LDLR</em>, <em>PCSK9</em>, and <em>LASER</em>, in peripheral blood mononuclear cells (PBMCs) of Iranian CAD patients in comparison to controls.</div></div><div><h3>Experimental approach</h3><div>This case-control study included 49 CAD patients, with 81.63 % receiving statins, compared to 40 control subjects, of whom 40 % received statins. The qRT-PCR was used to analyze the expression levels of <em>LDLR</em>, <em>PCSK9</em>, and <em>LASER</em> in PBMCs. Additionally, the ELISA method was employed to determine the blood concentration of PCSK9.</div></div><div><h3>Findings / results</h3><div>CAD patients demonstrated a significant reduction in PBMC gene expression levels of LDLR (P &lt; 0.01) and a significant rise in gene expression of <em>PCSK9</em> and <em>LASER</em>, as well as blood concentration of PCSK9 (P &lt; 0.05) compared to controls. The gene expression of <em>PCSK9</em> showed a strong positive relationship with <em>LDLR</em> expression in patients (P = 0.0003). Furthermore, a strong correlation was seen between <em>PCSK9</em> and <em>LASER</em>, as well as <em>LASER</em> and <em>LDLR</em> expression (P &lt; 0.0001) in two groups.</div></div><div><h3>Conclusion and implications</h3><div>PCSK9 and LASER are potential therapeutic targets for atherosclerosis-related disorders, including CAD. Given that patients receiving statins were twice that of the control subjects, and the effect of statins on the <em>LDLR</em>, <em>PCSK9</em> and <em>LASER</em>, further research is required to delineate the distinct effects of coronary artery disease conditions and statin usage on the expression of the aforementioned genes.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106969"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of COX inhibitor and arachidonic acid in manipulating obesity and obesity-induced bone resorption markers in obese mice","authors":"Rahima Begum,&nbsp;Sourav Roy,&nbsp;Md. Abdur Rahman Ripon,&nbsp;Mohammad Tohidul Amin,&nbsp;Mohammad Salim Hossain","doi":"10.1016/j.prostaglandins.2025.106971","DOIUrl":"10.1016/j.prostaglandins.2025.106971","url":null,"abstract":"<div><div>Obesity and bone-loss have remained a focus of research. Obesity stimulates adipose tissue expansion and adipocyte hypertrophy, resulting in chronic low-grade inflammation in the adipocytes. This enlarged adipocyte secretes a variety of pro-inflammatory chemicals. Because of their endocrine signaling, these substances indirectly promote osteoclast activity and bone-loss. However, the role of COX-2 signaling in obesity-induced bone resorption gene expression has yet to be investigated. Thus, we conducted this study in the context of obesity, employing a high-fat diet-induced obese mouse model. Obese mice treated with a selective and non-selective COX-2 inhibitor (celecoxib and aspirin), significantly (p &lt; 0.05) reduced adipogenic markers such as body and fat weight, serum lipids, mRNA expression of pro-inflammatory markers (COX-2, TNF-α, IL-6, and MCP-1) in adipose tissue and bone resorption markers (OPG, RANKL, Cathepsin K, and MMP-9) in tibia bone tissue. In addition, arachidonic acid (AA) supplementation significantly (p &lt; 0.5) increased the expression of obesity-induced inflammatory cytokines in the tibia bone marrow via the COX-2-derived PGE₂ signaling pathway, hence increase the osteoclastogenesis. These findings suggested that inhibiting the COX-2 signaling pathway could reduce obesity and inflammatory bone resorption. Although both the selective and non-selective COX inhibitors had similar effects, selective COX-2 was more effective in these events, indicating that COX-2 plays a critical role in obesity-associated inflammatory bone resorption.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106971"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143611011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aspirin-triggered RvD1 (AT-RvD1) modulates epithelial-mesenchymal transition on bronchial epithelial cells stimulated with cigarette smoke extract","authors":"Aline Beatriz Mahler Pereira ,&nbsp;Bethânia Alves Gontijo ,&nbsp;Sarah Cristina Sato Vaz Tanaka ,&nbsp;Fernanda Bernadelli de Vito ,&nbsp;Hélio Moraes de Souza ,&nbsp;Paulo Roberto da Silva ,&nbsp;Alexandre de Paula Rogerio","doi":"10.1016/j.prostaglandins.2025.106968","DOIUrl":"10.1016/j.prostaglandins.2025.106968","url":null,"abstract":"<div><div>The epithelial-mesenchymal transition (EMT) plays significant role in airway remodeling during chronic obstructive pulmonary disease (COPD) and lung cancer. Aspirin-triggered resolvin D1 (AT-RvD1) presents anti-inflammatory and pro-resolution effects, via lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2). In addition, AT-RvD1 prevented TGF-β1-induced EMT in lung cancer cells (A549 cells). Here, we extend these results and evaluated the role of AT-RvD1 in cigarette smoke extract (CSE)-induced EMT on bronchial epithelial cells (BEAS-2B). CSE decreased E-cadherin expression, an epithelial marker, and increased ROS and TGF-β1 productions, and expressions of mesenchymal markers (N-cadherin, vimentin, smad2/3 and slug). Furthermore, CSE induced an increase in the ALX/FPR2 receptor expression. AT-RvD1 restored the expression of E-cadherin and reduced the N-cadherin, Vimentin, smad2/3 and ALX/FPR2 expressions as well as ROS and TGF-β1 productions on CSE-stimulated cells. In conclusion, AT-RvD1 has the potential to control epithelial-mesenchymal transition induced by smoking in the normal lung epithelial cells.</div></div>","PeriodicalId":21161,"journal":{"name":"Prostaglandins & other lipid mediators","volume":"177 ","pages":"Article 106968"},"PeriodicalIF":2.5,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143453402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}